“First, by describing Fuddy as falling prey to a fatality of a non-fatal accident, I was making an intentional word play to underscore what I consider to be rather peculiar about the circumstances of Ms. Fuddy’s death.”
Okay, fair enough. What’s peculiar though? That she survived the crash but died in the ocean? I’d call that bad luck, but not very curious.
“I have not yet reached a final conclusion that Fuddy’s death involved anything more than an accident. To me, though it falls within the realm of “somewhat mysterious.” Those are the words I used in my post, not “shocking mystery, or breathtaking conspiracy,” etc. To which you responded “What’s so mysterious . . .”. Gee whiz, Mister. Sorry. Would it be okay if I described the matter as “a teensy bit eyebrow-raising”? Or would you swoop in to take exception with those words as well?”
Well, what is mysterious about it? Or peculiar, curious, or eyebrow-raising, or whatever you want to call it?
“In the same respect, isn’t the phrase “was killed” regularly used without any reference to conscious human agency as the cause?”
Yes, sure, but not “regularly” in the case of people who say “Fuddy was killed”. In that case, I would say it’s a quite rare phraseology.
While waiting for the toxicology report to complete the coroner’s report, I’ll speculate that cause of death for Loretta Fuddy is related to Stress-induced Sudden Cardiac Arrest.
Pardon the “medicalese” in the following but the bottom line is that any of us can inherit a genetic makeup that has us more prone to dying in an extremely stressful situation such as falling out of the sky and into the ocean.
Insight into stress-induced cardiomyopathy and sudden cardiac death due to stress. A forensic cardio-pathologist point of view.
Authors: Fineschi V, et al. Show all Journal
Forensic Sci Int. 2010 Jan 30;194(1-3):1-8. doi: 10.1016/j.forsciint.2009.10.025. Epub 2009 Nov 24.
Abstract
Emotional, physiological and physical stress is associated with increased rates of cerebrovascular events and sudden deaths. The pathophysiology of stress-induced cardiomyopathy is not well understood. Proposed mechanisms for catecholamine-mediated stunning in stress cardiomyopathy include epicardial vasospasm, microvascular dysfunction, hyperdynamic contractility with midventricular or outflow tract obstruction, and direct effects of catecholamines on cardiomyocytes. Studies show evidence of significant heritable influences on individual responses to adrenergic stimulation. Data from such studies may be of help for a more accurate comprehension of clinical and morphological alterations of the heart. Irrespective of the cause, patients with the classic stress-induced cardiomyopathy morphology deserve special attention because this extensive distribution of wall motion abnormalities has implications for potential associated complications. Cardiac response may be significantly coupled to genetic differences at candidate loci that encode components of catecholamine biosynthesis, storage, and metabolic pathway. Given the role of the sympathetic nervous system in responses to acute stress, it is reasonable to explore whether genetically determined alterations in catecholamine system functions contribute to acute and chronic cardiovascular disorders such as stress-induced cardiomyopathy.